Homocysteine-lowering therapy does not affect inflammatory markers of atherosclerosis in patients with stable

Ø Bleie1, A G Semb, H Grundt

  • 1Department of Heart Disease, Haukeland University Hospital, Bergen, Norway. oyvind.bleie@helse-bergen.no

Insights

Homocysteine-lowering B-vitamin therapy reduced homocysteine levels but did not impact key inflammatory markers linked to atherosclerosis in patients with stable coronary artery disease.

Area of Science:

  • Cardiovascular Disease Research
  • Nutritional Biochemistry
  • Inflammation Studies

Background:

  • Elevated total homocysteine (tHcy) is a recognized risk marker for cardiovascular disease (CVD) and is associated with inflammatory processes.
  • Inflammatory markers play a crucial role in the development of atherosclerosis.

Purpose of the Study:

  • To investigate the effect of B-vitamin therapy on inflammatory markers associated with atherosclerosis.
  • To assess whether homocysteine-lowering B-vitamin therapy influences inflammation in patients with suspected coronary artery disease (CAD).

Main Methods:

  • A prospective, double-blind, randomized 2x2 factorial clinical trial involving 90 patients with suspected CAD.
  • Patients received daily oral treatment with folic acid/vitamin B12/vitamin B6, folic acid/vitamin B12, vitamin B6 alone, or placebo for 6 months.
  • Blood samples were analyzed for tHcy and inflammatory markers (neopterin, sCD40L, IL-6, CRP) before and after treatment.

Main Results:

  • Homocysteine levels were significantly reduced by 33% in patients receiving folic acid/B12 (groups A and B) (P < 0.001).
  • tHcy showed significant positive associations with neopterin (r = 0.49, P < 0.001) and IL-6 (r = 0.29, P = 0.01).
  • B-vitamin treatments did not induce significant changes in neopterin, sCD40L, IL-6, or CRP levels (P >= 0.14).

Conclusions:

  • Homocysteine-lowering therapy using B-vitamins in patients with stable CAD does not alter inflammatory markers associated with atherogenesis.
  • The inability of B-vitamins to reverse inflammatory processes may contribute to the negative outcomes observed in secondary B-vitamin intervention trials for CVD.
Abstract

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